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Zhilyaev, S. Yu.; Moskvin, A. N.; Platonova, T. F.; Gutsaeva, Diana; Churilina, I V; Demchenko, Ivan T.

doi:10.1023/a:1025145331149

Cited by 65 publications

(29 citation statements)

References 17 publications

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“…SOD increased CBF in rats breathing air, but was ineffective after previous inhibition of NOS 76 . HBO induced CBF decreases, though prior SOD prevented hyperoxic vasoconstriction and increased CBF under HBO in rats.…”

Section: Hyperbaric Oxygen (Hbo) and Cbf Regulation By Enosmentioning

confidence: 87%

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Role of Endothelial Nitric Oxide in Cerebrovascular Regulation

Atochin

Huang²

2011

CPB

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Endothelial nitric oxide (NO) plays important roles in the vascular system. Animal models that show vascular dysfunction demonstrate the protective role of endothelial NO dependent pathways. This review focuses on the role of endothelial NO in the regulation of cerebral blood flow and vascular tone. We will discuss the importance of NO in cerebrovascular function using animal models with altered endothelial NO production under normal, ischemic and reperfusion conditions, as well as in hyperoxia. Pharmacological and genetic manipulations of the endothelial NO system demonstrate the essential roles of endothelial NO synthase in maintenance of vascular tone and cerebral perfusion under normal and pathological conditions.

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Section: Hyperbaric Oxygen (Hbo) and Cbf Regulation By Enosmentioning

confidence: 87%

“…The vasodilator effect of SOD in HBO was not observed in rats pretreated with NOS inhibitor. These results suggest inactivation of NO by superoxide anion as a mechanism of hyperoxic vasoconstriction [76] .…”

Section: Hyperbaric Oxygen (Hbo) and Cbf Regulation By Enosmentioning

confidence: 99%

Role of Endothelial Nitric Oxide in Cerebrovascular Regulation

Atochin

Huang²

2011

CPB

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“…Other effects of HBO, including stimulation of angiogenesis [33,34,35,36], and decreased cerebral edema and intracranial pressure [16,37,38,39,40], have also been suggested as mechanisms of protection from cerebral ischemia. These recent studies have shown several pathways as possible targets for neuroprotection from HBO, although a good deal of the data is preliminary and needs to be replicated and expounded upon before a clear picture will arise as to the true mechanisms of HBO.…”

Section: Mechanism Of Action Of Hbomentioning

confidence: 99%

Hyperbaric Oxygen Therapy of Cerebral Ischemia

Helms

Whelan

Torbey³

2005

Cerebrovasc Dis

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Background: Hyperbaric oxygen (HBO) therapy of cerebral ischemia has been evaluated in a number of human and animal studies; however, there is presently no consensus on its efficacy. Methods: We present a review of animal and human studies on HBO therapy of cerebral ischemia as well as present potential mechanisms of action of HBO. Results: Animal studies of HBO have shown promise by reducing infarct size and improving neurologic outcome. HBO has also been shown to inhibit inflammation and apoptosis after cerebral ischemia. Early reports in humans also suggested benefit in stroke patients treated with HBO. Recent randomized, controlled human studies, however, have not shown benefit, although all were limited by small sample size. Important differences between animal and human studies suggest HBO might be more effective in stroke within the first few hours and at a pressure of 2–3 ATA. Conclusions: The clinical usefulness of HBO in the treatment of cerebral ischemia is not yet certain. Attention to emerging pathophysiologic data should be taken into consideration in design of any future clinical trials of HBO in acute ischemic stroke.

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“…Moreover, eNOS may not be inhibited in the early period of exposure, although CBF decreased rapidly after the oxygen pressure was raised. As suggested by Demchenko et al and Zhilyaev et al this transient decrease was mainly resulted from inactivation of eNOS-dependent NO by •O 2 − , decreasing the basal vasorelaxing action of NO 17,18…”

Section: Discussionmentioning

confidence: 86%

“…However, it was different on the point that which NOS isoform played a more important role in the modulation of the later vasodilation. Some considered NO by eNOS was responsible for the development of hyperoxic hyperemia preceding O 2 seizures, whereas neuronal NO may mediate toxic effects of HBO mainly by its reaction with superoxide to generate the stronger oxidant, peroxynitrite 18. Others suggested late HBO-induced vasodilation depends upon NO produced by both eNOS and nNOS 5.…”

Section: Discussionmentioning

confidence: 99%

Endothelial Nitric Oxide Synthase Expression Is Progressively Increased in Primary Cerebral Microvascular Endothelial Cells During Hyperbaric Oxygen Exposure

Zhongzhuang

et al. 2008

Oxidative Medicine and Cellular Longevity

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Exposure to hyperbaric oxygen (HBO) can lead to seizures. Many studies have demonstrated that there exist a very close relationship between the alteration of cerebral blood flow (CBF) and the onset of seizures. Nitric oxide (NO) may play a key role in the change of CBF during exposure, and modulation of endothelial nitric oxide synthase (eNOS)-derived NO by HBO is responsible for early vasoconstriction, whereas late HBO-induced vasodilation depends upon a large amount of NO from both eNOS and neuronal nitric oxide synthase (nNOS). To investigate the effect of HBO on the activity and expression of eNOS in cerebral microvascular endothelial cells (CMEC) in vitro, primarily cultured CMEC from neonatal rats were exposed to oxygen at 500 kPa [5 atmosphere absolute (ATA)] for 10, 20, 30, 60 and 120 minutes (min), then eNOS activity, protein and mRNA contents in cells were detected. Our results showed that immediately after exposure, 30, 60 and 120 min HBO exposures did not alter NOS activity. When detected no matter immediately or six hours (h) after exposure, these exposures also did not alter eNOS protein and mRNA levels. However, when detected 24 h after exposure, 30, 60 and 120 min exposures upregulated eNOS protein content by 39%, 60% and 40% respectively. 10 and 20 min exposures upregulated eNOS mRNA content by about 15%, while 30, 60 and 120 min exposures upregulated it by about 20–30%. The increased eNOS protein and mRNA contents at 24 h after exposure may reflect new protein synthesis for eNOS. Our studies showed that with the exposing protocols we used, HBO did induce eNOS expression increase in CMEC. However, compared with the decrease of CBF in vivo, which occurred in a relative short time after rat was exposed to HBO above 4 ATA, the responses of eNOS in CMEC in vitro were a little slow. Thus we considered that for the vasodilation in the late period of HBO exposure before seizure, the effect of NO produced by eNOS was limited.

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Untitled

Cited by 65 publications

References 17 publications

Role of Endothelial Nitric Oxide in Cerebrovascular Regulation

Role of Endothelial Nitric Oxide in Cerebrovascular Regulation

Hyperbaric Oxygen Therapy of Cerebral Ischemia

Endothelial Nitric Oxide Synthase Expression Is Progressively Increased in Primary Cerebral Microvascular Endothelial Cells During Hyperbaric Oxygen Exposure

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